Dyslexia: is it genetic and what does this mean for social inclusion?

Abstract

Purpose

This paper starts by considering what it means if dyslexia has genetic or environmental causes. The author also explains phrases used by genetic researchers and the kind of things they look for in genetic material. The purpose of this paper is to discuss two recent studies on dyslexia that shed light on either genetic or environmental causes.

Design/methodology/approach

One study was a thorough exploration of possible genetic differences that could be present in children experiencing reading and language difficulties. The other study examined a large sample of the Canadian public to see whether there was a link between dyslexia and having experienced physical abuse as a child or teenager.

Findings

The study on genetic differences found no evidence for some previously suggested genetic causes of dyslexia. Although previous studies have suggested dyslexia runs in families, the genetic contribution may have been overestimated. The study on the Canadian public found that people who reported experiencing physical abuse in their younger years were six to seven times more likely also to have a diagnosis of dyslexia. Childhood trauma is known to affect brain development.

Originality/value

Although this paper only discusses two papers in detail, they are two of the most recent explorations of genetic and environmental links to dyslexia. There could be a case for greater attention to possible traumatic experiences in children identified as dyslexic. Physical abuse is one possibility but should never be assumed. Families can be under strain and may need more support. However, dyslexia and the mental health difficulties that can result from childhood trauma can reduce a child’s current and future social inclusion. Early intervention may avert this outcome.

Citation

Holttum, S. (2016), "Dyslexia: is it genetic and what does this mean for social inclusion?", Mental Health and Social Inclusion, Vol. 20 No. 4, pp. 202-207. https://doi.org/10.1108/MHSI-08-2016-0024